> How so? And more importantly how much antibiotics make it to the gut, vs if you take it orally? I would guess it would be a lot less.
I have no idea what figure or percentage it would be, but for most common antibiotics which end up distributed in total body water, there will be a component that leaks into the gut through capillary action; if it is metabolised in the liver then a proportion of it will end up in bile (if fat soluble) and then enter the gut that way; either itself or a metabolite of it - it would be impossible for me to quantify and likely depends on many many factors such as molecular weight, structure and a host of other features.
Patients on IV antibiotics develop diarrhoea from IV antibiotics at a similar rate (from what I have experienced) to those on orals. hence it undoubtedly kills bacteria in a similar fashion.
And we use IV antibiotics to kill bad infections of the gut. So whatever the mechanism, if I have elucidated it or simply done some hand-waving, it clearly affects it significantly.
The only instance of antibiotic use that touches on what I feel you are pushing for is the use of oral vancomycin (It is almost always IV) for severe bacterial infections of the gut - we use it oral because it is not absorbed systemically (as opposed to other specifically oral antibiotics) so doesn't cause systemic effects.
> then spreads through horizontal gene transfer.
Sure. But if you look at how they tested this particular antibiotic for the ability to develop resistance, they exposed TB and Staph to sub-theraputic doses for 27 days, or (for Staph) or 810generations (assuming a rough rate of division somewhere around 40 min to 1 hr in ideal conditions). An epic number of cell divisions if you work it out (and I can't).
The commonly accepted knowledge, as far as I understand it and as far as I have been taught it, whether or not bowel bacteria have a significant role to play or not, is that exposure of antibiotics to sub-lethal doses for long periods of time promote the survival of strains that have a competitive advantage against the agent in use, which over time allows the strain to survive in otherwise-lethal doses, and that gene becomes incorporated into a plasmid and then ends up spreading to every other organism capable of horizontal gene transfer.
Anyway, I am at home and not going to see the next MD, PhD in Infectious Diseases until tomorrow but when I do I will ask him and reply here. So, check back in 24 hours if you're interested
On the off-chance that you read this I apologise for not delivering, I wasn't able to speak to ID but will on Monday so if this thread is locked by then then shoot me an email
I have no idea what figure or percentage it would be, but for most common antibiotics which end up distributed in total body water, there will be a component that leaks into the gut through capillary action; if it is metabolised in the liver then a proportion of it will end up in bile (if fat soluble) and then enter the gut that way; either itself or a metabolite of it - it would be impossible for me to quantify and likely depends on many many factors such as molecular weight, structure and a host of other features.
Patients on IV antibiotics develop diarrhoea from IV antibiotics at a similar rate (from what I have experienced) to those on orals. hence it undoubtedly kills bacteria in a similar fashion.
And we use IV antibiotics to kill bad infections of the gut. So whatever the mechanism, if I have elucidated it or simply done some hand-waving, it clearly affects it significantly.
The only instance of antibiotic use that touches on what I feel you are pushing for is the use of oral vancomycin (It is almost always IV) for severe bacterial infections of the gut - we use it oral because it is not absorbed systemically (as opposed to other specifically oral antibiotics) so doesn't cause systemic effects.
> then spreads through horizontal gene transfer.
Sure. But if you look at how they tested this particular antibiotic for the ability to develop resistance, they exposed TB and Staph to sub-theraputic doses for 27 days, or (for Staph) or 810generations (assuming a rough rate of division somewhere around 40 min to 1 hr in ideal conditions). An epic number of cell divisions if you work it out (and I can't).
The commonly accepted knowledge, as far as I understand it and as far as I have been taught it, whether or not bowel bacteria have a significant role to play or not, is that exposure of antibiotics to sub-lethal doses for long periods of time promote the survival of strains that have a competitive advantage against the agent in use, which over time allows the strain to survive in otherwise-lethal doses, and that gene becomes incorporated into a plasmid and then ends up spreading to every other organism capable of horizontal gene transfer.
Anyway, I am at home and not going to see the next MD, PhD in Infectious Diseases until tomorrow but when I do I will ask him and reply here. So, check back in 24 hours if you're interested